鼠伤寒沙门氏菌感染小鼠会通过自然杀伤细胞依赖途径诱导一氧化氮介导的免疫抑制。
Salmonella typhimurium infection in mice induces nitric oxide-mediated immunosuppression through a natural killer cell-dependent pathway.
作者信息
Schwacha M G, Meissler J J, Eisenstein T K
机构信息
Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, Pennsylvania 19140, USA.
出版信息
Infect Immun. 1998 Dec;66(12):5862-6. doi: 10.1128/IAI.66.12.5862-5866.1998.
Abstract
Splenocytes isolated from C57BL/6J female mice 3 to 7 days after inoculation with an attenuated strain of Salmonella typhimurium produced high levels of nitric oxide (39 to 77 microM) and gamma interferon (IFN-gamma). Additionally, spleen cell cultures from Salmonella-inoculated mice were markedly suppressed in their ability to generate an in vitro plaque-forming cell (PFC) response to sheep erythrocytes. Depletion of natural killer (NK) cells from the immune splenocyte population markedly reduced nitric oxide production, prevented suppression of PFC responses, and completely abrogated IFN-gamma release. Treatment of NK cell-depleted immune cells with IFN-gamma restored nitric oxide production to levels comparable to those of intact immune cells and also restored the immunosuppression. These results suggest that NK cells regulate the induction of nitric oxide-mediated immunosuppression following infection with S. typhimurium through the production of IFN-gamma.
摘要
用减毒鼠伤寒沙门氏菌接种C57BL/6J雌性小鼠3至7天后分离的脾细胞产生高水平的一氧化氮（39至77微摩尔）和γ干扰素（IFN-γ）。此外，来自接种沙门氏菌小鼠的脾细胞培养物对绵羊红细胞产生体外空斑形成细胞（PFC）反应的能力受到明显抑制。从免疫脾细胞群体中去除自然杀伤（NK）细胞可显著降低一氧化氮的产生，防止PFC反应受到抑制，并完全消除IFN-γ的释放。用IFN-γ处理去除NK细胞的免疫细胞可将一氧化氮的产生恢复到与完整免疫细胞相当的水平，同时也恢复了免疫抑制作用。这些结果表明，NK细胞通过产生IFN-γ来调节鼠伤寒沙门氏菌感染后一氧化氮介导的免疫抑制的诱导。
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